Endodontic Infections Quiz

Endodontic Microbiology Introduction

• Microbes are the primary cause of pulp and periapical tissue pathologies.
• Effective endodontic treatment necessitates recognizing the cause of microbial invasion.
• Understanding microbes associated with endodontic disease helps develop a basic understanding of disease processes and sound management strategies.

Can Normal Flora Cause Disease?

• Oral microbiome varies between individuals but is generally similar across humans.
• Commensal oral flora typically exists in symbiotic harmony with the host.
• Disease arises when microbial equilibrium is disrupted (dysbiosis).
• Transient flora seldom establishes itself in the oral environment due to colonization resistance exerted by resident flora.

Stages of Root Canal Infection

• Microbes enter the pulp.
• Pulp tissue becomes necrotic.
• Pulp loses its blood supply.
• A reservoir of microbes and their products accumulates.
• This climax of the community is a significant stage.

Rate of Bacterial Invasion

• Bacterial invasion increases with time.
• Initial invasion rate is approximately 1.6 µm/day within the first 25 days.
• Invasion rate then increases to 14 µm/day by 120 days.
• Deepest bacterial invasion (3.0 mm) occurs approximately 210 days post-surgery.

A Historical View

• Antonie van Leeuwenhoek (17th century) described oral microflora, observing plaque in exposed dental cavities.
• W.D. Miller (1890) is considered the father of oral microbiology, linking oral microorganisms to pulpal disease.

Etiological Factors in Pulp and Periradicular Diseases

• 1965: Kakehashi et al. identified bacteria as the primary etiological factors for pulpal and periradicular diseases.
• Studies showed that without bacterial involvement, exposure of dental pulp exhibited only minor inflammation.
• 1976: Sundqvist used various culturing techniques to identify and classify bacteria and concluded that root canal infections are a result of multiple bacterial species.

Portals of Entry for Microorganisms

• Under healthy conditions, the pulpodentin complex is isolated from oral microbiota by enamel, dentin, and cementum.
• Caries lesions, saliva, and dental plaque introduce microbes to exposed areas of the pulpodentin complex.
• Periodontal disease-associated microorganisms can access the pulp via dentinal tubules at the cervical part of the tooth.

Dentin Exposure and Pulp Infection Risk

• Dentin exposure places pulp at risk of infection due to dentin permeability via its tubular structure.
• Dentinal tubule diameter varies, largest near the pulp (mean 2.5 µm) and smallest at the periphery (mean 0.9 µm).
• Most oral bacteria range in size from 0.2-0.7 µm, which is compatible with dentinal tubule diameters.

Routes of Root Canal Infection

• Caries, trauma, faulty restorations, and diseases like gingivitis can cause root canal infections.
• Dental scaling, root planning procedures, subgingival plaque biofilms, apical and lateral accessory foramina are key entryways for bacterial infection.
• Vitality of the pulp influences susceptibility. Vital pulp is protected from bacterial invasion, while necrotic pulp is easily infected.

Microbial Penetration During and After Treatment

• Biofilm remnants and calculus exacerbate infection risk during treatment.
• Caries in the crown and leaking rubber dams can introduce microbes.
• Contaminated instruments, irrigant solutions, and open dressing present further risks during treatment.
• Post-treatment complications occur due to leakage via restorations and delayed placement.
• Recurrent decay in the root canal is an especially concerning post-treatment setback.

Pulp Necrosis and Primary Endodontic Infections

• Necrosis of the dental pulp is a necessary prerequisite for establishing primary endodontic infections, whatever the route of bacterial access.

Sources of Nutrients for Colonizing Bacteria

• Necrotic pulp tissue provides nutrients to colonizing bacteria.
• Tissue fluids and exudates rich in proteins and glycoproteins seep into the root canal via apical and lateral foramina.
• Saliva and products of other bacteria's metabolism contribute to nutrient sources.

Classification of Microorganisms

• Gram-positive microorganisms include Streptococcus, Actinomyces, Enterococcus, Lactobacillus, Treponema, and Candida.
• Gram-negative microorganisms include Fusobacterium, Neisseria, Campylobacter, Bacteroides, and Veillonella.

Oxygen Requirements of Microorganisms

• Obligate aerobes require oxygen for growth.
• Facultative anaerobes can survive in the presence or absence of oxygen.
• Microaerophilic bacteria thrive in oxygenated environments but metabolically function in the absence of oxygen.
• Obligate anaerobes require the absence of oxygen for growth.

Microbial Ecosystem of the Root Canal

• Gram-positive organisms are common in root canals, but gram-negative and obligate anaerobes are also present.
• Necrotic pulp lacks circulation, hindering host defense mechanisms, and serving as a reservoir for invading microbes.

Organisms Commonly Found in Endodontic Infections

• Bacteroides (various species), Streptococcus, Enterococcus, Lactobacilli, Actinomyces, Yeasts, Tannerella forsythia, and Fusobacterium nucleatum are common.

Microflora of Traumatized/Intact Teeth with Necrotic Pulp

• Bacteria like B. melaninogenicus, Eubacterium yurii, and other bridging oral species (F. nucleatum, Corynebacterium) commonly associated with traumatized teeth.
• Species like Bacteroides, Porphyromonas, Prevotella, and other microorganisms associated with acute endodontic infections.

Endodontic Flare-Up Infections

• Obligate anaerobic microbes like Veillonella, Capnocytophaga, Eiknela, Bacteroides, Fusobacterium, and Treponema are involved in endodontic flare-ups.
• Refractory endodontic cases frequently exhibit E. faecalis, Candida albicans, and Actinomyces israelii.

Microflora of Infected/Untreated Necrotic Pulp

• Common inhabitants include Fusobacterium, Porphyromonas gingivalis, Prevotella intermedius, Eubacterium, and Peptostreptococcus.
• Previously root-filled teeth with apical periodontitis show presence of Actinomyces, Enterococcus, and Propionibacterium.

Mechanisms of Microbial Pathogenicity and Virulence Factors

• Pathogenicity describes an organism's capacity to cause disease.
• Virulence signifies the degree of pathogenicity, with virulence factors enabling pathogenicity.
• Primary pathogens typically and readily cause disease.
• Opportunistic pathogens cause disease under compromised host defenses.

Virulence Factors

• Lipopolysaccharides (LPS) are surface components of gram-negative bacteria.
• LPS are nonspecific antigens not neutralized by antibodies.
• Extracellular vesicles, produced by gram-negative bacteria, can be endotoxins, outer membrane fragments, or blebs.
• Bacterial enzymes facilitate infection spread, immunoglobulin neutralization, and complement component neutralization.

Additional Virulence Factors

• Fatty acids (e.g., propionic acid, butyric acid) produced by anaerobic bacteria promote bone resorption and periradicular diseases.
• Polyamines are biologically active molecules in infected canals, impacting cell growth, tissue regeneration, and inflammation.
• Pili facilitate bacterial adhesion and interaction with other bacteria.
• Bacterial capsules enable resistance to phagocytosis in various gram-negative bacteria.

Types of Endodontic Infections

• Intraradicular infections are categorized into primary (initial or virgin), secondary (introduced after treatment), and persistent (resistant to treatment), categorized in turn as symptomatic or asymptomatic.
• Extraradicular infections are independent or dependent on intraradicular infections.

Primary Intraradicular Infections

• Gram-negative anaerobes (e.g., Prevotella, Fusobacterium, Tannerella, Dialister, Porphyromonas, Campylobacter, Treponema) frequently cause primary intraradicular infections.
• Gram-positive anaerobes (e.g., Peptostreptococcus, Eubacterium, Actinomyces) and facultative/microaerophilic streptococci are also possible primary pathogens.

Symptomatic Infections

• Specific microorganisms have not been indicated to cause symptomatic endodontic diseases.
• Factors like bacterial numbers, environmental cues, bacterial interactions, differences in virulence play a role in disease etiology, preceding the onset of symptoms.
• Microbial succession and pathogenicity degrees determine inflammation, triggering symptoms like pain or swelling.

Asymptomatic Infections

• Before symptoms appear, microbial community structures adjust.
• New pathogens appear, existing ones change, affecting dominant species and overall species diversity in root canals.
• These shifts, lacking a defining pathogen, contribute to symptom development.

Persisters After Intracanal Disinfection

• Microorganisms that survived intracanal disinfection are often involved in persistent endodontic infections.
• Fungi (Candididae) are often more prevalent than in primary infections following treatment.

Enterococcus faecalis

• Gram-positive, facultative anaerobic coccus commonly associated with endodontic infections.
• Often a significant component of root canal failures.
• Survives in root canals as a major component of the flora.
• Resistant to starvation, adheres to dentin and tubules, suppressing the action of lymphocytes, utilizing serum, resisting intracanal medications, and forming biofilms.

Enterococcus faecalis (Continued)

• High prevalence (40%) observed in primary and (24-77%) in persistent infections.
• Significantly more resistant to phagocytosis, antibodies, and antimicrobials than related species.
• This bacterium can readily survive in alkaline environments and has a tolerance of 10-45°C and 60°C for 30 minutes.
• Frequently detected in asymptomatic, compared to symptomatic cases (Roca et al).

Extraradicular Infections

• Microorganisms invade periradicular tissues, overcoming the body's defense mechanisms.
• Actinomyces, Streptococcus, and P. propionicum are common in extraradicular infections.
• Infection is dependent on pre-existing intraradicular factors.
• Infections can result from intraradicular complications (e.g., over-instrumentation, debris extrusion, or acute alveolar abscesses).

Biofilms

• Biofilm is defined as a microbial community firmly attached to a surface or a self-produced extracellular polymeric matrix.
• Bacterial biofilms are prevalent in apical root canals of teeth with primary or post-treatment periapical periodontitis.

Endodontic Biofilms

• Endodontic microflora show less diversity compared to oral microflora; they persist in complex anatomical and geometrical areas of root canals, which protect them from cleanup procedures.
• Bacterial activities don't exclusively occur within the canals; they extend beyond apical foramina.

Biofilm Development

• Biofilms develop through planktonic bacterial cell attachment to superficial surfaces.
• Microbial growth and biofilm expansion occur, followed by detachment and planktonic growth of microbial components.

Intracanal, Extraradicular, and Periapical Biofilms

• Biofilms form on root canal dentin.
• They occur on root surfaces and cementum, adjacent to root apexes.
• The isolated species in periapical areas include Actinomyces and Porphyromonas propionicum.
• Presence of sulfur granules and frequent presence in refractory periapical lesions are noted.

Biomaterial-Centered Infections (BCI)

• Bacteria adhere to artificial materials (e.g., root canal obturators), forming biofilms.
• Proximity to the host immune system exacerbates susceptibility to BCI.
• Common BCI isolates include coagulase-negative Staphylococci, S. aureus, enterococci, P. aeruginosa, and various fungi.
• BCI has 3 phases: transport to the surface, non-specific adhesion, and specific adhesion.

Microbiological Diagnostic Techniques

• Diagnostic techniques include culture, microscopy, immunology, and molecular methods to identify microbial agents causing endodontic issues.

Microbial Sampling from the Root Canal

• Microbial sampling methods include initial (diagnostic), intermediate, and final samplings and methods like sampling through canals (e.g., collecting with paper points, aspirating into anaerobic mediums, disinfecting tooth surfaces).

How to Combat Microbes

• Thorough cleaning and shaping of the root canal system coupled with 3-dimensional obturation are important.
• Irrigants like sodium hypochlorite eliminate bacteria from canal irregularities.
• Oxygenating agents can be helpful but should be used cautiously to prevent periapical tissue infection.

Abscesses, Drainage, and Antibiotics

• Tooth exudate (serous, purulent, or hemorrhagic) should be handled under supervision to support canal drainage.
• Abscesses, potent irritants, generate elevated osmotic pressure attracting fluid, exacerbating edema and pain.
• Drainage through canals or soft tissue can ease inflammation.
• Antibiotics are an adjunct especially in severe infections, guided by the types of root canal microorganisms.

Intracanal Medications

• Medicaments such as calcium hydroxide play a crucial role in combating bacteria in necrotic pulps.
• Use of these medicaments enhances treatment outcomes post-root canal instrumentation.

Influence of Microbiology on Endodontic Failure

• E. faecalis is a key microorganism associated with endodontic failure; however, recent studies highlight roles of other bacteria like Fusobacterium nucleatum and Propionibacterium in endodontic failure situations.

Microbial Assessment in Root Canals

• Studies assessed Gram-positive vs. Gram-negative bacteria in root canals with necrosis, finding no statistically significant difference in bacterial counts between the groups.
• The findings suggested a mixed microbiota in such cases.

Antimicrobial Efficacy of Chitosan, Chlorhexidine, Propolis, and Sodium Hypochlorite

• Combination of chlorhexidine and chitosan demonstrated comparable effectiveness against E. faecalis biofilms.
• Similar to chlorhexidine-chitosan combinations, sodium hypochlorite demonstrated comparable efficacy.
• Studies showed a similar level of antimicrobial action for propolis.

Comparative Efficacy of Endodontic Medicaments and Sodium Hypochlorite

• Sodium hypochlorite showed total bacterial eradication against E. faecalis biofilms.
• Other treatments (Ledermix, Odontopaste, Ca(OH)2, combinations) exhibited less complete bacterial reduction (in viability) compared to sodium hypochlorite.

Conclusion: Oral Flora

• Oral microorganisms are frequently commensals; however, environmental changes can make them pathogenic.
• Maintaining a healthy balance between oral microbes and the host is crucial to maintain oral commensal balance.